ATRIAL FIBRILLATION
Supraventricular ectopy and recurrence of atrial fibrillation after electrical cardioversion
Department of Cardiology, Westmead Hospital, Cnr Hawkesbury and Darcy Rds, Westmead NSW 2145, Australia
Manuscript submitted 9 August 2005. Accepted after revision 15 January 2006.
* Corresponding author. Tel: +61 2 9845 6795; fax: +61 2 9845 8323. E-mail address: stuartpt{at}yahoo.com
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Abstract |
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Aims Paroxysmal atrial fibrillation (AF) is usually preceded by a premature atrial complex (PAC). We hypothesized that patients with a high frequency of atrial ectopic activity after restoration of sinus rhythm following direct current cardioversion would be more likely to experience recurrence of AF.
Methods and results Forty-four patients with documented persistent AF were studied. A 24 h Holter recording was performed from the day of external direct current cardioversion. Patients were reviewed at 1 week, 1 month, and 6 months. After 6 months, 59% of patients had experienced a recurrence of AF. Neither the frequency of PACs nor the frequency or duration of supraventricular tachycardia (SVT) episodes predicted AF recurrence (P=0.60, 0.30, and 0.42, respectively). There was a trend towards maximum rate of SVT predicting recurrence of AF (P=0.08).
Conclusion Frequency of supraventricular ectopy or the number and length of SVT runs in the 24 h after restoration of sinus rhythm are not strong predictors of recurrence of AF after electrical cardioversion. A larger study would be required to detect a small predictive effect.
Key Words: Atrial fibrillation, Supraventricular ectopy, Cardioversion
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Introduction |
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Persistent atrial fibrillation (AF) may be terminated by transthoracic electrical cardioversion but recurrence of AF is common.1
,2 Pharmacological therapy can reduce the risk of AF recurrence but carries a risk of adverse reactions and may not be tolerated. Knowledge of factors that predict recurrence of AF after electrical cardioversion may allow tailoring of therapy for specific groups of AF patients. More aggressive therapy may be appropriate for patients at a higher risk of AF recurrence. Several factors have been identified that predict the risk of AF recurrence after electrical cardioversion including prolonged duration of AF,3–5 increased left atrial size,3–5 underlying heart disease,3,4 and increased heart rate variability.6 However, the predictive value of these risk factors is limited.
Intermittent AF is precipitated by ectopic activation of the atria from the pulmonary veins in the majority of cases. However, the role of the pulmonary veins in persistent AF is less clear. Atrial tachycardia or focal ectopic beats initiate AF.7,8 Furthermore, focal atrial arrhythmias in the 2 min immediately following internal electrical cardioversion are common in persistent AF and have been shown to predict early AF recurrence.9 We hypothesized that patients with frequent premature atrial complexes (PACs) or atrial arrhythmia in the 24 h after external electrical cardioversion would be more likely to have recurrence of AF.
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Methods |
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Patient selection and study procedure
Consecutive consenting patients referred to our unit for electrical cardioversion of persistent AF between July 2001 and October 2002 were included in this study. Persistent AF was defined as AF present continuously for at least 1 week. Forty-four patients who underwent successful cardioversion to sinus rhythm were enrolled in the study. Stable sinus rhythm was determined by electrocardiographic means immediately following the procedure and prior to discharge later the same day. Intracardiac thrombus was excluded in all patients by transoesophageal echocardiographic assessment. Electrical cardioversion was performed under deep sedation. Patients remained on their existing medications after the procedure, including any antiarrhythmic or anticoagulant agents. During the same admission within 1 h of cardioversion, a 24 h Holter recording (Del Mar Avionics, CA, USA) was obtained. Patients were reviewed at 1 week, 1 month, and 6 months to determine the presence and timing of AF recurrences. This was determined by performing a 12-lead electrocardiogram on the day of follow up. The study was approved by the Western Sydney Human Research and Ethics Committee.
ECG analysis
Multi-channel 24 h Holter (ambulatory) ECG data from each patient were acquired digitally and transferred for computerized analysis. The individual event traces and digital analysis were reviewed and reported by an electrophysiologist blinded to the clinical outcome. Premature atrial complexes were defined as beats falling within a normal beat cluster but with rate 
80 bpm and prematurity 20% of the preceding beat. Supraventricular tachycardia (SVT) was defined as three or more sequential PACs. The maximum SVT rate was the highest rate in beats per minute of any SVT run. Maximum PAC per minute was the greatest number of PACs occurring in any 1 min period and similarly maximum PAC per hour was the greatest number of PACs occurring in any 60 min period. Atrial fibrillation was considered present on ECG criteria where P-waves were not detectable and irregular fibrillatory waves were present with a rate >350 bpm.
Statistical analysis
A significance level of 5% was used throughout the analysis. The clinical and demographic data, together with the presence, nature, and frequency of ectopic beats and SVT, were used as the explanatory variables in univariate comparisons. The dichotomous outcome variable was AF recurrence at any stage within the 6 months follow-up. 
2 tests were used to test for association between the categorical variables and the outcome variable. Mann–Whitney tests were used to test for association between the continuous or ordered categorical variables and the dichotomous outcome variable.
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Results |
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The mean age of the group was 70.8±10.3 years. Twelve patients (27%) had ischaemic heart disease, 19 (43%) had valvular dysfunction, 12 (27%) had abnormal left ventricular function, 37 (84%) had left atrial enlargement, and 25 (57%) had hypertension. Twenty-seven patients (61%) had a known history of paroxysmal AF of less than 3 months, 2 patients (5%) had a known history between 3 and 6 months and 15 (34%) had a known history of paroxysmal AF of more than 6 months. Fifteen patients (34%) had documented electrical or chemical cardioversion previously at least once.
Twenty-one patients (48%) were on rate-controlling medications (metoprolol, carvedilol, bisoprolol, diltiazem, verapamil, and digoxin) and 30 (68%) on rhythm-controlling medications (amiodarone, sotalol, and flecainide) at the time of cardioversion. Eleven patients (25%) had antiarrhythmic medications changed during the follow-up period with three patients having medications added, four having medications withdrawn, and three having both medications added and withdrawn.
Twenty-six patients (59%, Group A) experienced a recurrence of AF during the follow-up period of 6 months (32% by 1 week, 48% by 1 month, and 59% by 6 months) (Figure 1). The baseline clinical and echocardiographic data for Group A (patients developing AF in follow-up) and Group B (patients who remained in sinus rhythm) are shown in Table 1. None of these baseline variables predicted the recurrence of AF.
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The Holter data are shown in Table 2. The number of PACs, rate of supraventricular ectopy, and runs of supraventricular events (including total tachycardia) did not predict recurrence of AF (Figure 2). However, a trend towards significance was seen for maximum rate of SVT.
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Discussion |
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The present study suggests that ambulatory Holter monitoring parameters such as frequency of atrial ectopy, presence of non-sustained SVT, and duration of SVT are not strong predictors of AF recurrence after electrical cardioversion. There are two possible explanations for this finding. First, there may be specific qualities of atrial ectopy required to initiate AF. Secondly, the substrate for atrial propensity to AF may be a more important factor than initiating mechanisms in our group of patients. Finally, the study was not sufficiently powered to detect a small effect. However, such an effect is not likely to be clinically useful when considering individual patient management.
Role of atrial ectopy in initiating AF
Previous studies have demonstrated that PACs are a common initiating factor for AF in the immediate period prior to the arrhythmia commencing.10–12 However, no other studies have focused on ectopy in the 24 h after electrical cardioversion. Todd et al.9 and, more recently, Raitt et al.13 have shown that focal atrial arrhythmias and PACs can predict AF recurrence. However, both these studies looked at the immediate period following cardioversion. Our study found no relationship between ectopic activity in the 24 h after cardioversion and recurrence of AF. A possible explanation for this observation is that only some patterns of atrial ectopic activity may trigger AF. Atrial ectopic activity may be characterized by particular coupling to the previous sinus beat (prematurity of the ectopic beat), interbeat coupling intervals, duration, and origin. Waktare et al.12 used Holter monitoring to show that PACs immediately preceding paroxysmal AF initiation were more premature and more frequent than PACs occurring at other times.
In the present study, ectopy and SVT were observed. However, there were no cases of AF during the monitoring period. The trend towards significance for SVT rate as a predictor of AF recurrence raises the possibility that these patients may continue to experience runs of rapid SVT and that such triggers are more likely to induce AF at a later date.
Role of atrial substrate in recurrence of AF
The initiation of AF requires a trigger that is almost invariably PACs or atrial tachycardia. However, not all patients with atrial arrhythmias will develop AF. Therefore, a suitable substrate for development of AF (i.e. vulnerable atrial myocardium) must co-exist with a suitable trigger. Previous studies have demonstrated that underlying heart disease or left atrial size increases the risk of AF recurrence after electrical cardioversion.3–5 These characteristics may influence trigger activity but they are also likely to be markers of an altered atrial substrate.
The balance between trigger and substrate is likely to be important. A particularly vulnerable substrate may allow the development of AF with a trigger that would not be arrhythmogenic in other less vulnerable atria. Animal models of AF clearly demonstrate that changes in the structure or functional changes within the atria alter the atrial vulnerability to development of AF during atrial programmed stimulation.14–16 Animal and human studies demonstrated that electrophysiological properties of atrial tissue can be changed by the presence of AF, increasing the atrial vulnerability to the arrhythmia.14–17 Thus, the vulnerability of the atrial substrate to a given trigger is dynamic and may undergo temporal fluctuations. The failure to demonstrate a relationship between duration of AF, left atrial size, and the presence of underlying structural heart disease and AF recurrence in the present study may be due to a combination of insufficient power and the relative homogeneity of the cohort.
Study limitations
The nature of follow-up at 1 week, 1 month, and 6 months intervals to determine recurrence of AF will miss patients with asymptomatic and self-terminating episodes between follow-up periods. However, although this phenomenon is well described in patients with intermittent AF, it is less common in patients with persistent AF.
Very many patients in our study were receiving antiarrhythmic medications, which may have influenced the degree and nature of atrial ectopy. Further, several patients had pharmacological regimes changed during the study period. The sample size studied was too small to evaluate the effects of these changes or individual drugs.
Our patient cohort was older and had a larger proportion with structural heart disease than previous studies. This may affect comparison with previous results.
Clinical relevance
The number of PACs, rate of supraventricular ectopy, and number of runs of supraventricular events were all higher in the group with AF recurrence. It is possible that a larger study may show that these factors have a small predictive value. However, the wide range of these variables in each group (Table 2) suggests that they are unlikely to be clinically useful for the prediction of recurrence in individual patients.
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Conclusion |
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The number of PACs, rate of supraventricular ectopy, and runs of supraventricular events (including total tachycardia) in the 24 h after electrical cardioversion from AF to sinus rhythm are not strong predictors of subsequent AF recurrence. Recurrence of AF depends on the presence of an arrhythmogenic trigger and a vulnerable substrate, which could not be predicted using the methods employed in this study.
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References |
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